Nuclear migration is an important developmental step in many organisms and can determine cell shape and size. Nuclear migration may also he required for cell migration, and therefore for proper brain development and for the spread of cancer. The filamentous fungus Aspergillus nidulans has excellent cytology and is amenable to genetic and biochemical approaches to studying nuclear migration. In this organism, three key participants in nuclear migration have been identified: microtubules, the microtubule motor dynein, and a protein similar to one involved in a human neuronal migration disease. The main goal of this proposal is to characterize a suppressor mutation (snf890) which improves nuclear migration for several migration-defective Aspergillus mutants. The phenotypes of the snf890 mutation suggest that it destabilizes microtubules and the mutation maps very close to the tubA tubulin gene. Specifically, the aim is to determine whether the snf890 gene is tubA and whether the suppressor mutation itself affects nuclear migration, nuclear division, or microtubule stability. Further experiments test mechanisms by which the snf890 mutation could suppress nuclear migration defects. In addition, a search for new suppressors may identify more participants in nuclear migration. Finally migration- defective mutants will be examined for abnormalities in the microtubule cytoskeleton. These experiments will enhance our understanding of nuclear migration and possibly other microtubule-mediated processes such as mitosis.